Dr. Sebastian Werneburg earned his B.Sc. in Biology from the Leibniz University Hannover, Germany, his M.Sc. in Biomedicine from the Hannover Medical School, Germany, and his summa cum laude awarded Ph.D. in Neuroscience from the University of Veterinary Medicine Hannover, Germany. Working with Dr. Herbert Hildebrandt as a graduate student, he conducted research on glial biology, neuroinflammation, and CNS repair as a member of the Institute for Clinical Biochemistry at Hannover Medical School. He then joined Dr. Dorothy Schafer’s group as a postdoc at the University of Massachusetts Chan Medical School in Worcester, USA, where he identified microglia-mediated synapse elimination as separable pathology underlying visual circuit dysfunction in demyelinating disease and developed a gene therapy approach to block synapse elimination and preserved circuit function in the visual system. In September 2022, Dr. Werneburg joined the Department of Ophthalmology and Visual Sciences at the University of Michigan, Michigan Health, as an Assistant Professor, where he continues to study glial biology, neuroinflammatory pathways, and the mechanisms underlying the de- and regeneration of neural circuits in neurodegenerative diseases with a special emphasis on the visual system in mouse models of Multiple Sclerosis.
Areas of Interest
Research in the Werneburg Lab focuses on understanding neuron-glia interactions and how these contribute to neuroinflammation and the de- and regeneration of neural circuits in neurological disorders. In particular, we are interested in the crosstalk between microglia, synapses, and inflammatory signaling pathways and how this communication affects circuit function in the visual system in mouse models of Multiple Sclerosis and related neurodegenerative diseases. The goal of our research is to unravel new cellular and molecular targets and develop strategies for therapeutic interventions that can halt progressive circuit degeneration or improve recovery – processes that are only insufficiently targeted by available disease-modifying therapies. To address these questions, the lab uses cutting-edge molecular, genetic, and omic approaches combined with high-resolution static and live confocal imaging.
Keywords: microglia, synapses, neuron-glia interactions, visual system, neural circuits, degeneration, regeneration, demyelinating disease, Multiple Sclerosis, neuroimmunology, complement signaling
- Werneburg S, Jung J, Kunjamma RB, Ha SK, Luciano NJ, Willis CM, Gao G, Biscota NP, Havton LA, Crocker SJ, Popko B, Reich DS, Schafer DP. Targeted complement inhibition at synapses prevents microglial synaptic engulfment and synapse loss in demyelinating disease. Immunity. 2020 Jan;14;52(1):167-182e.7. doi: 10.1016/j.immuni.2019.12.004. PMID: 31883839
- Schirmer L*, Velmeshev D*, Holmqvist S, Kaufmann M, Werneburg S, Jung D, Vistnes S, Stockley JH, Young A, Steindel M, Tung B, Goyal N, Bhaduri A, Mayer S, Broder Engler J, Franklin RJM, Haeussler M, Reynolds R, Schafer DP, Friese MA, Shiow LR, Kriegstein AR, Rowitch DH. Neuron subtype vulnerability and multilineage spatial diversity in multiple sclerosis. Nature. 2019 Sep;573(7772):75-82. doi: 10.1038/s41586-019-1404-z. PMID: 31316211
- Werneburg S, Feinberg PA, Johnson KM, Schafer DP. A microglia-cytokine axis to modulate synaptic connectivity and function. Curr Opinion Neurobiology. 2017. Dec;47:138-145. doi: 10.1016/j.conb.2017.10.002. PMID: 29096242
- Werneburg S, Fuchs HLS, Albers I, Burkhardt H, Gudi V, Skripuletz T, Stangel M, Gerardy-Schahn R, Hildebrandt H. Polysialylation at Early Stages of Oligodendrocyte Differentiation Promotes Myelin Repair. J Neuroscience. 2017. Aug 23;37(34):8131-8141. doi: 10.1523/JNEUROSCI.1147-17.2017. PMID: 28760868